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New Hypothesis Proposed for Cause of Chronic Fatigue Syndrome

February 1, 1999

COLUMBUS, Ohio - Researchers here have proposed a new theory for the cause of chronic fatigue syndrome (CFS) - one that blames the illness both on a low-level viral infection and on the body's own immune response to that virus.

The hypothesis was included in a paper published in the current issue of the American Journal of Medicine.

The new theory, proposed by Ronald Glaser, professor of medical microbiology and immunology, and Janice Kiecolt-Glaser, professor of psychology and psychiatry at Ohio State University, is the latest work in more than two decades of their research on the effects of stress on the human immune system.

"Our data suggests that stress may be causing the expression of certain viral proteins and that these proteins may be modulating the body's immune response, turning it on or off," Glaser said. The Ohio State researchers' new theory poses several mechanisms that might be linked to CFS.

Once a person is infected, these viruses can remain latent in the body for long periods of time. Glaser proposes that the viruses could be partially reactivated, that is, viral proteins could be produced at levels high enough to cause a low-grade infection but too low to be seen using current laboratory assays.

Glaser and Kiecolt-Glaser suggest that CFS patients may experience an ongoing, low-grade viral infection - more like a smoldering fire rather than a three-alarm blaze - which could stimulate parts of the immune response without raising antibody titers to typically high levels. That low-grade infection would be enough to increase production of various cytokines - chemical mediators for the immune system - and begin the immune response.

"A lot of the symptoms that you find in chronic fatigue syndrome are the same ones induced by cytokines during our normal immune response," Glaser said. These symptoms include fatigue, malaise, depression, and cognitive problems. He admits that studies of patients have yet to show a pattern of abnormal cytokine behavior that would substantiate their theory, for which he presents the following: "We haven't discovered all the cytokines involved in immunity. We may not have found the right one, yet," he said, adding that new cytokines are steadily being identified.

Stress and depression caused by the illness may be playing a related role as well, Kiecolt-Glaser said. Earlier research has repeatedly shown that increased stress and depression can reactivate latent viruses, decrease the body's immune response, and stimulate the production of certain cytokines linked to some CFS-like symptoms.

Although studies have indicated the onset of CFIDS is not related to depression or other psychiatric problems, it is evident that CFIDS can be a self-facilitating disease due to the tremendous stress experienced by those who suffer from it.

This research supports findings of CFIDS clinicians that stress can significantly exacerbate symptoms and therefore should be avoided.











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